EXTRAMYOCARDIAL ACIDOSIS IMPAIRS CARDIAC RESUSCITABILITY IN ISOLATED,PERFUSED, RAT HEARTS

Objectives: Patients suffering out-of-hospital cardiac arrest have var ious degrees of acidemia when cardiopulmonary resuscitation is initiat ed. Myocardial hypercarbia, rather than decreases in myocardial pH, ma y determine cardiac resuscitability. Accordingly, we questioned whethe r different degrees of acidemia accompanying cardiac arrest affect car diac resuscitability. We evaluated the effect of different degrees of extramyocardial acidosis on cardiac performance and resuscitability af ter ventricular fibrillation using isolated, perfused, rat hearts. Des ign: Prospective, randomized, controlled study. Setting: Experimental animal laboratory in a university hospital. Subjects: Thirty one male, Sprague-Dawley rats. Interventions: Rat hearts were perfused with N-[ 2-hydroxyethyl]piperazine-N-[2-ethanesulfonic acid] (HEPES) buffered s olution (sodium chloride 145 mM, potassium chloride 4 mM, sodium dihyd rogen phosphate dihydrate 1.25 mM, magnesium chloride 1.5 mM, calcium chloride 2 mM, HEPES 6 mM, glucose 10 mM), which was bubbled with 100% oxygen and adjusted to a pH of 7.4. The perfusion pressure was held c onstant at 60 mm Hg. After 60 mins of stabilization, the control perfu sion solution was switched to one of the solutions titrated to pH 6.2, 6.5, 6.8, 7.1, or 7.4, using 1 N of sodium hydroxide. Hearts were all ocated randomly to each group. After 15 mins of perfusion, the perfusi on was discontinued, and artificial ventricular fibrillation was induc ed by electrical stimulation for 5 mins. The hearts were then perfused again in one of the same acidotic solutions for 30 mins. Measurements and Main Results: Left ventricular developed pressure (left ventricul ar pressure minus end-diastolic left ventricular pressure), positive c hange in left ventricular pressure over time, heart rate (HR), and cor onary flow were continuously measured. After 60 mins of stabilization, the values of left ventricular developed pressure, positive change in left ventricular pressure over time, HR, and coronary flow were not s ignificantly different between groups. After 5 mins of ventricular fib rillation, all hearts were asystolic and left ventricular developed pr essure, positive change in left ventricular pressure over time, HR, an d coronary flow were all zero. After 30 mins of reperfusion, all value s in the acidotic groups were significantly lower than the values in t he pH 7.4 group. When we judged the recovery of left ventricular devel oped pressure at >35 mm Hg as ''resuscitated,'' resuscitability was im paired at a pH of <7.1. No hearts recovered after perfusion below a pH of 6.5. Conclusions: Extramyocardial acidosis below pH 7.1 decreased cardiac performance and resuscitability after ventricular fibrillation . This result indicates that progressive acidemia during cardiac arres t is one of the important determinants of cardiac resuscitability.